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理解自闭症中的抑郁症:主观感知与前扣带回皮质体积的作用。

Understanding Depression in Autism: The Role of Subjective Perception and Anterior Cingulate Cortex Volume.

作者信息

Hao Yu, Banker Sarah, Trayvick Jadyn, Barkley Sarah, Peters Arabella, Thinakaran Abigael, McLaughlin Christopher, Gu Xiaosi, Foss-Feig Jennifer, Schiller Daniela

机构信息

Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

出版信息

Res Sq. 2024 Sep 20:rs.3.rs-4947599. doi: 10.21203/rs.3.rs-4947599/v1.

DOI:10.21203/rs.3.rs-4947599/v1
PMID:39372931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11451742/
Abstract

BACKGROUND

The prevalence of depression is elevated in individuals with autism spectrum disorder (ASD) compared to the general population, yet the reasons for this disparity remain unclear. While social deficits central to ASD may contribute to depression, it is uncertain whether social interaction behavior themselves or individuals' introspection about their social behaviors are more impactful. Although the anterior cingulate cortex (ACC) and amygdala are frequently implicated in ASD, depression, and social functioning, it is unknown if these regions explain differences between ASD adults with and without co-occurring depression.

METHODS

The present study contrasted observed vs. subjective perception of autism symptoms and social performances assessed with both standardized measures and a lab task, in 65 sex-balanced (52.24% male) autistic young adults. We also quantified ACC and amygdala volume with 7-Tesla structural neuroimaging to examine correlations with depression and social functioning.

RESULTS

We found that ASD individuals with depression exhibited differences in subjective evaluations including heightened self-awareness of ASD symptoms, lower subjective satisfaction with social relations, and less perceived affiliation during the social interaction task, yet no differences in corresponding observed measures, compared to those without depression. Larger ACC volume was related to depression, greater self-awareness of ASD symptoms, and worse subjective satisfaction with social interactions. In contrast, amygdala volume, despite its association with clinician-rated ASD symptoms, was not related to depression.

LIMITATIONS

Due to the cross-sectional nature of our study, we cannot determine the directionality of the observed relationships. Additionally, we included only individuals with an IQ over 60 to ensure participants could complete the social task, which excluded many on the autism spectrum. We also utilized self-reported depression indices instead of clinically diagnosed depression, which may limit the comprehensiveness of the findings.

CONCLUSIONS

Our approach highlights the unique role of subjective perception of autism symptoms and social interactions, beyond the observable manifestation of social interaction in ASD, in contributing to depression, with the ACC playing a crucial role. These findings imply possible heterogeneity of ASD concerning co-occurring depression. Using neuroimaging, we were able to demarcate depressive phenotypes co-occurring alongside autistic phenotypes.

摘要

背景

与普通人群相比,自闭症谱系障碍(ASD)个体中抑郁症的患病率有所升高,但这种差异的原因尚不清楚。虽然ASD核心的社交缺陷可能导致抑郁症,但社交互动行为本身或个体对其社交行为的内省哪个影响更大尚不确定。尽管前扣带回皮质(ACC)和杏仁核经常与ASD、抑郁症和社交功能有关,但尚不清楚这些区域是否能解释伴有或不伴有抑郁症的成年ASD患者之间的差异。

方法

本研究对比了65名性别均衡(52.24%为男性)的自闭症青年成人中,通过标准化测量和实验室任务评估的自闭症症状及社交表现的观察结果与主观认知。我们还通过7特斯拉结构神经成像对ACC和杏仁核体积进行了量化,以研究其与抑郁症和社交功能的相关性。

结果

我们发现,与无抑郁症的ASD个体相比,伴有抑郁症的ASD个体在主观评价上存在差异,包括对ASD症状的自我意识增强、对社会关系的主观满意度较低,以及在社交互动任务中感受到的归属感较低,但在相应的观察指标上没有差异。ACC体积较大与抑郁症、对ASD症状的更强自我意识以及对社交互动的更差主观满意度有关。相比之下,杏仁核体积尽管与临床医生评定的ASD症状有关,但与抑郁症无关。

局限性

由于我们研究的横断面性质,我们无法确定所观察到的关系的方向性。此外,我们仅纳入了智商超过60的个体,以确保参与者能够完成社交任务,这排除了许多自闭症谱系中的个体。我们还使用了自我报告的抑郁指数而非临床诊断的抑郁症,这可能会限制研究结果的全面性。

结论

我们的方法突出了自闭症症状和社交互动的主观认知在导致抑郁症方面的独特作用,这超出了ASD中社交互动的可观察表现,其中ACC起着关键作用。这些发现意味着ASD在伴发抑郁症方面可能存在异质性。通过神经成像,我们能够区分与自闭症表型同时出现的抑郁表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/e37effcd5a5d/nihpp-rs4947599v1-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/8964730c6f5a/nihpp-rs4947599v1-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/2a438fce8659/nihpp-rs4947599v1-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/e37effcd5a5d/nihpp-rs4947599v1-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/8964730c6f5a/nihpp-rs4947599v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/e79cd99cf2d5/nihpp-rs4947599v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/392d0634f67d/nihpp-rs4947599v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/35411da6cf2e/nihpp-rs4947599v1-f0006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37c/11451742/e37effcd5a5d/nihpp-rs4947599v1-f0009.jpg

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